Postprandial Insulin Levels Research Articles

Suppressing adipocyte inflammation promotes insulin resistance in mice

ObjectiveObesity-induced insulin resistance is closely associated with chronic subclinical inflammation in white adipose tissue. However, the mechanistic involvement of adipocyte-derived inflammation under these disease conditions remains unclear. Our aim was to investigate the relative inflammation-related contributions of adipocytes and macrophages to insulin sensitivity. MethodsRIDα/β is an adenoviral protein complex that inhibits several inflammatory pathways, including TLR4, TNFα, and IL1β signaling. We generated novel mouse models with adipocyte-specific and macrophage-specific doxycycline (dox)-inducible RIDα/β-transgenic mice (RIDad and RIDmac mice, respectively). ResultsRIDα/β induction significantly reduced LPS-stimulated inflammatory markers, such as Tnf, Il1b, and Saa3 in adipose tissues. Surprisingly, RIDad mice had elevated levels of postprandial glucose and insulin and exhibited glucose intolerance and insulin resistance, even under chow-fed conditions. Moreover, the RIDad mice displayed further insulin resistance under obesogenic (high-fat diet, HFD) conditions despite reduced weight gain. In addition, under pre-existing obese and inflamed conditions on an HFD, subsequent induction of RIDα/β in RIDad mice reduced body weight gain, further exacerbating glucose tolerance, enhancing insulin resistance and fatty liver, and reducing adiponectin levels. This occurred despite effective suppression of the inflammatory pathways (including TNFα and IL1β). In contrast, RIDmac mice, upon HFD feeding, displayed similar weight gain, comparable adiponectin levels, and insulin sensitivity, suggesting that the inflammatory properties of macrophages did not exert a negative impact on metabolic readouts. RIDα/β expression and the ensuing suppression of inflammation in adipocytes enhanced adipose tissue fibrosis and reduced vascularization. ConclusionOur novel findings further corroborate our previous observations suggesting that suppressing adipocyte inflammation impairs adipose tissue function and promotes insulin resistance, despite beneficial effects on weight gain.

Predictors of the Acute Postprandial Response to Breaking Up Prolonged Sitting.

To identify predictors of favorable changes to postprandial insulin and glucose levels in response to interrupting prolonged sitting time with standing or light-intensity physical activity. Data were combined from four similarly designed randomized acute cross-over trials (n = 129; body mass index [BMI] range, 19.6-44.6 kg·m; South Asian = 31.0%; dysglycemia = 27.1%). Treatments included: prolonged sitting (6.5 h) or prolonged sitting broken-up with either standing or light-intensity physical activity (5 min every 30 min). Time-averaged postprandial responses for insulin and glucose were calculated for each treatment (mean ± 95% confidence interval). Mutually adjusted interaction terms were used to examine whether anthropometric (BMI), demographic (age, sex, ethnicity [white European vs South Asian]) and a cardiometabolic variable (Homeostatic Model Assessment of Insulin Resistance)-modified responses. Postprandial insulin and glucose were reduced when individuals interrupted prolonged sitting with bouts of light physical activity, but not with standing. Reductions in time-averaged postprandial insulin were more pronounced if individuals were South Asian compared with white European (-18.9 mU·L [-23.5%] vs -8.2 mU·L [-9.3%]), female compared with male (-15.0 mU·L [-21.2%] vs -12.1 mU·L [-17.6%]) or had a BMI ≥27.2 kg·m (-20.9 mU·L [-22.9%] vs -8.7 mU·L [-18.2%]). Similarly, being female (-0.4 mmol·L [-0.6 mmol·L, -0.2 mmol·L], -6.8% vs -0.1 mmol·L [-0.3 mmol·L, 1 mmol·L], -1.7%) or having a BMI ≥27.2 kg·m (-0.4 mmol·L [-0.6 mmol·L, -0.2 mmol·L], -6.7% vs -0.2 mmol·L [-0.4 mmol·L, 0.0 mmol·L], -3.4%) modified the postprandial glucose response. No significant interactions were found for Homeostatic Model Assessment of Insulin Resistance or age. Being female, South Asian, or having a higher BMI, all predicted greater reductions in postprandial insulin, whereas being female and having a higher BMI predicted greater reductions in postprandial glucose when sitting was interrupted with light physical activity. These results could help to guide personalized interventions in high-risk participants for whom breaking prolonged sitting time with light activity may yield the greatest therapeutic potential.

Reduced Insulin Clearance and Insulin-Degrading Enzyme Activity Contribute to Hyperinsulinemia in African Americans.

African Americans (AAs) are at a higher risk for developing type 2 diabetes compared with non-Hispanic whites (NHWs). The causal role of β-cell glucose sensitivity (β-GS) and insulin clearance in hyperinsulinemia in AA adults is unclear. Using a cross-sectional study design, we compared β-cell function and insulin clearance in nondiabetic AAs (n = 36) and NHWs (n = 47) after a mixed meal test (MMT). Insulin secretion rate, glucose sensitivity, rate sensitivity, and insulin sensitivity during MMT were derived from a mathematical model. Levels of insulin-degrading enzyme (IDE) and carcinoembryonic antigen-related cell adhesion molecule-1 (CEACAM1), key players in insulin clearance, were measured (by enzyme-linked immunosorbent assay) in hepatic cytosolic fractions from age-, sex-, and body mass index-matched AA and NHW cadaveric donors (n = 10). Fasting and mean postprandial plasma glucose levels were similar in both ethnic groups. AAs had significantly higher fasting and mean postprandial plasma insulin levels. However, fasting ISR, total insulin output, and insulin sensitivity during MMT were not different between the groups. β-GS and rate sensitivity were higher in AAs. Fasting and meal plasma insulin clearance were lower in AAs. Hepatic levels of IDE and CEACAM-1 were similar in AAs and NHWs. Hepatic IDE activity was significantly lower in AAs. In this study, lower insulin clearance contributes to higher plasma insulin levels in AAs. Reduced insulin clearance may be explained by lower IDE activity levels in AAs. Further confirmatory studies are needed to investigate diminished insulin clearance in AAs as a result of lower IDE activity levels.

Preliminary examination of insulin and amylin levels in women with purging disorder.

This preliminary study explored whether differences in meal-stimulated insulin or amylin release are linked to altered ingestive behaviors in individuals with bulimia nervosa (BN) or purging disorder (PD). Women with BN (n = 15), PD (n = 16), or no eating disorder (n = 18) underwent structured clinical interviews and assessments of gut hormone and subjective responses to a fixed test meal. Multilevel model analyses were used to explore whether gut hormone responses contribute to subjective responses to the test meal and whether these associations differed by group. Insulin and amylin levels significantly increased following the test meal. Women with PD showed greater insulin release compared to those with BN, but not controls. Multilevel models support significant group X insulin interactions predicting subjective ratings of nausea and urge to vomit, with a stronger association between higher insulin responses and higher nausea and urge to vomit in women with PD and BN. Amylin responses did not differ by group. Increased sensitivity to the effects of insulin on nausea and urge to vomit may be linked to purging in both PD and BN. Differences in postprandial insulin levels may be linked to purging behavior in the absence versus presence of binge eating.

Effect of High β-glucan Barley on Postprandial Blood Glucose and Insulin Levels in Type 2 Diabetic Patients

The aim of our study was to investigate whether high β-glucan-containing barley (7.2 g per 100 g) improves postprandial plasma glucose levels and suppresses postprandial insulin levels during a meal tolerance test in type 2 diabetic patients. A meal tolerance test (500 kcal) was conducted using two types of test meals: a test meal with white rice (WR) alone (WR diet) and a test meal with WR mixed with 50% barley (BR diet) as staple food. The side dish was the same in the both meals. The changes in plasma glucose and serum C-peptide immunoreactivity (CPR) levels for 180 minutes after ingestion of the test meals were compared. Ten patients with type 2 diabetes (age 52.5 ± 15.1 years, and 7 males and 3 females) were included in this study. The mean HbA1c level and body mass index were 8.8 ± 1.4%, and 29.7 ± 4.5 kg/m2, respectively. Plasma glucose levels after ingestion of the WR diet or BR diet peaked at 60 minutes, which showed no significant differences between the two types of test meals. However, the incremental area under the curve (IAUC) of plasma glucose levels after ingestion of BR diet was significantly lower than that of WR diet. The serum CPR levels at 180 min and their IAUC over 180 minutes after ingestion of BR diet were significantly lower than those of WR diet. Conclusion: Increase in postprandial plasma glucose and insulin levels was suppressed by mixing high-β-glucan barley with WR in type 2 diabetic patients.

Consuming coffee with milk and sugar added before a high glycemic index meal improves postprandial glycemic and insulinemic responses

AbstractLiterature regarding the health effect of coffee consumption was contradicting, whereby it was found to protect against type 2 diabetes while inducing acute glucose intolerance. Previous studies suggested that adding sugar and milk into coffee may alter the effect of its consumption on glucose metabolism, potentially explaining the contradiction, but this is seldom investigated. This study aimed at assessing the effect of adding milk and sugar into coffee on the postprandial glycemic metabolism after a subsequent, high glycemic index (GI) meal. A total of 11 apparently healthy adults were recruited for this randomized, cross-over acute feeding study. In each experimental session, overnight-fasted participants consumed one cup of the following drinks: espresso (35 ml), instant, boiled, and decaffeinated coffee (all 150 ml). Then they consumed a high GI meal and blood samples were collected every 15–30 minutes in the subsequent two hours. Each type of coffee was tested for 3 times, twice with 50 g low-fat milk and 7.5 g white sugar added (i.e. white coffee) and once without (i.e. black coffee). Postprandial levels of glucose, insulin, and active GLP-1, as well as the incremental area-under-curve (iAUC) of the biomarkers, were compared between black and white coffee, with baseline measurements as a covariate. Results showed that the peak glucose level after the meal was lower in white coffee sessions than black coffee sessions, regardless of coffee types. The difference was the greatest between black and white decaffeinated coffee (mean difference from baseline ± SEM, white coffee: 2.5 ± 0.2 mmol/L; black coffee: 3.3 ± 0.3 mmol/L, p = 0.019). The mean glucose iAUC of white coffee sessions was significantly smaller than black coffee sessions for all coffee types except for instant coffee (all p < 0.05). The peak insulin levels between black and white coffees were not significantly different, yet white decaffeinated coffee had a 35% smaller mean insulin iAUC than black decaffeinated coffee (p = 0.025). The active GLP-1 levels were not significantly different between black and white coffee sessions. These results showed that prior ingestion of coffee with milk and sugar added attenuated the glucose response after the subsequent meal, compared with drinking black coffee beforehand. Our results may provide an explanation for the conflicting literature regarding the protective effects of coffee consumption against type 2 diabetes.

The carbohydrate-insulin model does not explain the impact of varying dietary macronutrients on the body weight and adiposity of mice

ObjectivesThe carbohydrate-insulin model (CIM) predicts that increases in fasting and post-prandial insulin in response to dietary carbohydrates stimulate energy intake and lower energy expenditures, leading to positive energy balance and weight gain. The objective of the present study was to directly test the CIM's predictions using C57BL/6 mice. MethodsDiets were designed by altering dietary carbohydrates with either fixed protein or fat content and were fed to C57BL/6 mice acutely or chronically for 12 weeks. The body weight, body composition, food intake, and energy expenditures of the mice were measured. Their fasting and post-prandial glucose and insulin levels were also measured. RNA-seq was performed on RNA from the hypothalamus and subcutaneous white adipose tissue. Pathway analysis was conducted using IPA. ResultsOnly the post-prandial insulin and fasting glucose levels followed the CIM's predictions. The lipolysis and leptin signaling pathways in the sWAT were inhibited in relation to the elevated fasting insulin, supporting the CIM's predicted impact of high insulin. However, because higher fasting insulin was unrelated to carbohydrate intake, the overall pattern did not support the model. Moreover, the hypothalamic hunger pathways were inhibited in relation to the increased fasting insulin, and the energy intake was not increased. The browning pathway in the sWAT was inhibited at higher insulin levels, but the daily energy expenditure was not altered. ConclusionsTwo of the predictions were partially supported (and hence also partially not supported) and the other three predictions were not supported. We conclude that the CIM does not explain the impact of dietary macronutrients on adiposity in mice.

Antidiabetic effect of withanolides and liraglutide on serum insulin level and pancreatic histology in diabetic rats.

Objectives: Type 2 diabetes is characterized by hyperglycemia and occurs as a result of insulin resistance and pancreatic beta cells failure to compensate. Present study was conducted to determine the antidiabetic effect of Withania coagulans and liraglutide on postprandial serum insulin levels and pancreatic histological features in streptozotocin induced diabetic rat. Study Design: This Randomized Control Trial. Setting: At multidisciplinary lab Islamic International Medical College, Rawalpindi in collaboration with Animal House, National Institute of Health, Islamabad. Period: From March 2016 to April 2017. Material and Methods: Forty male Sprague daily rats were randomly divided into normal Control Group A (n=10) and Experimental Group (n=30). Experimental group was given streptozotocin (30mg/kg/day) intraperitoneally for 5 days and diabetes was confirmed in experimental group by measuring fasting blood glucose level (mg/dl). Experimental group was divided further into Group B (Diabetic control), Group C (Withania coagulans treated) and Group D (Liraglutide treated). Group C were given Withania coagulans in addition to normal diet and Group D received Liraglutide besides normal diet for 30 days. Second sampling for evaluating postprandial serum insulin level and pancreatic histology was done after 30 days. Result: Postprandial serum insulin levels of Withania coagulans treated Group C (5.54 + 0.23 μU/ml) and Liraglutide treated Group D (6.06 + 0.17 μU/ml) were significantly raised in comparison with Diabetic control Group B (3.50 + 0.19 μU/ml), whereas islets of Langerhans cell morphology were markedly improved in Group C and D as compared to Group B. Conclusion: Withania coagulans significantly increases postprandial serum insulin level and improves pancreatic beta cells architecture.

KCa3.1 channel mediates inflammatory signaling of pancreatic β cells and progression of type 2 diabetes mellitus.

Chronic islet inflammation is associated with development of type 2 diabetes mellitus (T2DM). Intermediate-conductance calcium-activated K+ (KCa3.1) channel plays an important role in inflammatory diseases. However, the role and regulation of KCa3.1 in pancreatic β cells in progression of T2DM remain unclarified. In the present study, we evaluated the effect of the specific KCa3.1 channel blocker 1-[(2-chlorophenyl)diphenylmethyl]-1H-pyrazole (TRAM-34) on diabetic phenotype in the db/db model. In diabetic mice, blockade of KCa3.1 significantly improved glucose tolerance, enhanced secretion of postprandial insulin level, and reduced loss of β-cell mass through attenuating the expression and secretion of inflammatory mediators. Furthermore, in cultured pancreatic β cells, exposure to high levels of glucose or palmitic acid significantly increased expression and current density of the KCa3.1 channel as well as secretion of proinflammatory chemokines, and the effects were similarly reversed by preincubation with TRAM-34 or a NF-κB inhibitor pyrrolidinedithiocarbamate. Additionally, expression of KCa3.1 in pancreas islet cells was up-regulated by activation of NF-κB with IL-1β stimulation. In summary, up-regulated KCa3.1 due to activation of NF-κB pathway leads to pancreatic inflammation via expression and secretion of chemokines and cytokines by pancreatic β cells, thereby facilitating progression of T2DM.-Pang, Z.-D., Wang, Y., Wang, X.-J., She, G., Ma, X.-Z., Song, Z., Zhao, L.-M., Wang, H.-F., Lai, B.-C., Gou, W., Du, X.-J., Deng, X.-L. KCa3.1 channel mediates inflammatory signaling of pancreatic β cells and progression of type 2 diabetes mellitus.

Glycemic and Insulinemic Responses of Vegetables and Beans Powders Supplemented Chapattis in Healthy Humans: A Randomized, Crossover Trial.

Vegetables and beans are nutrient-dense foods with innate potential to mediate diabetes in a variety of cultures. The present study aims at evaluating vegetables and beans for assessing their glycemic index and response in raising glucose levels in human model. Powdered formulations of vegetables and beans were designed to modulate glycemic response of carbohydrate-rich staples. A randomized, crossover trial was conducted in healthy young adults (n = 24) who were challenged with vegetable powder-supplemented chapatti (VPSC), bean powder-supplemented chapatti (BPSC) and all-purpose wheat flour chapatti (APFC) to evaluate their postprandial glucose (PPG) and postprandial insulin (PPI) responses. In comparison with APFC, feeding VPSC and BPSC to healthy volunteers anticipated significant reduction in PPG (44% reduction in incremental area under the curve (AUC) for VPSC and 46% reduction in incremental AUC for BPSC, p = 0.005). Likewise, significant reduction in PPI levels was observed for VPSC (59%, p = 0.012) and BPSC (47%, p = 0.002) compared to APFC-treated group. The study concludes wheat flour enrichment with vegetables and beans powder as a viable approach to develop cost effective and culturally acceptable low glycemic foods bearing acceptable sensory attributes.

Effect of vegetable juice consumption prior to eating rice on postprandial blood glucose and insulin levels.

Vegetable juice has been demonstrated to attenuate the elevation of postprandial blood glucose when consumed prior to meals. The present study aimed to investigate the effect of pre-meal consumption of vegetable juice on blood glucose and insulin levels. A total of 10 healthy volunteers aged 20–29 years ingested 200 ml of either water, a sugar solution with the same sugar composition as the vegetable juice or vegetable juice 30 min prior to consuming the cooked rice, and their blood glucose and insulin levels were measured. At the time of rice consumption and 15 min thereafter, blood glucose and plasma insulin levels tended to be lower in the vegetable juice intake group compared with those in the sugar solution intake group. However, there were no significant differences in the kinetic parameters (incremental area under the glucose curve and maximum change in glucose concentration) between these two groups. These results suggest that the sugars contained in vegetable juice account for the suppression of postprandial hyperglycemia.

Critical and emerging topics in dietary carbohydrates and health

Multiple factors may affect the metabolic fate of carbohydrates. Today, well-standardised and accepted methods may allow for the definitions of the changes in the glucose and insulin curves following the ingestion of either carbohydrate-based and other foods. More debate is still raised on the clinical meaning of these classifications when used at a population level, while emphasis is raised on the approach to carbohydrate metabolism on an individual basis. Within these ranges of applications, other compounds, such as plant polyphenols, may favourably add synergic effects through the modulation of carbohydrate digestion and glucose metabolic steps, resulting in lowering postprandial glucose and insulin levels. Finally, a growing knowledge suggests that the balance of dietary fructose and individual physical activity represent the key point to address the compound towards either positive, energy sparing effects, or a degenerative metabolic burden. The carbohydrate quality within a whole dietary and lifestyle pattern may therefore challenge the individual balance towards health or disease.

Hematologic and Serological Investigation of Effect on Gyeongokgo in Healthy Individuals : a Randomized, Subject-assessor-blind, Placebo-controlled, Single-center Pilot Study

There are no published data on Gyeongokgo (GOK) safety or efficacy despite being commonly use. The Gyeongokgo (GOK) is commonly used in traditional Korean medicine to promote a health qi and blood, but their objective data was not sufficient in clinical field. To investigate the safety and efficacy of GOK with hematologic and serologic testing and the change of the quality of life in healthy individuals. Randomized, subject-assessor-blind, placebo-controlled, single-center pilot study Participants and Interventions 29 healthy volunteer subjects were randomly placed into the GOK group (n = 20) or placebo control group (n = 9) and instructed to take one treatment packet (GOK or placebo) twice daily for 4 weeks. Subjects were assessed using the Fatigue Severity Scale (FSS) and Short Form 36 Health Survey (SF-36) and underwent hematologic and serologic tests and body composition analysis. The FSS total score (p = 0.093) and SF-36 general health index (p = 0.002) were improved following treatment in the GOK group. Post-treatment thyroid-stimulating hormone levels were increased in the GOK group compared with pre-treatment levels (p = 0.0042). C-reactive protein levels decreased (p = 0.0256) in the GOK group compared with that the placebo group. In time-series tests, GOK did not affect post-prandial serum triglycerides, glucose, insulin, or C-peptide levels. Notably, elevations in serum fasting triglycerides at 2- (p = 0.0333) and 4-hours (p = 0.0414) post-prandial were lower than those in the placebo group. GOK reduced fatigue levels and did not significantly affect laboratory test results performed to measure safety, serum glucose, and lipid profiles. Post-meal triglyceride levels were effectively reduced with treatment.

The role of Leu260Phe polymorphism of the receptor gene to GLP-1 incretin in the pathogenesis of diabetes type 2 diabetes with obesity

BACKGROUND: Glucagon-like peptide-1 (GLP-1) stimulates the proliferation of β-cells, enhances their resistance to apoptosis and increases glucose-dependent insulin secretion. AIMS: Study of the relationship of Leu260Phe polymorphism (rs1042044) of the GLP-1R gene with postprandial hormone production (C-peptide, insulin, ghrelin, GLP-1) in obese patients with type 2 diabetes. MATERIALS AND METHODS: A total of 174 patients, 82 patients with obesity with type 2 diabetes (BMI=40.4±14.3 kg/m 2 )and 92 conditionally healthy donors (BMI=22.6±2.7 kg/m 2 ) were studied. The material for the study was venous blood taken on an empty stomach and 60 minutes after the test breakfast. Genotyping was performed by PCR using the sets for determining polymorphism (rs1042044) of the GLP-1R gene (Sintol) and the amplificator (CFX96 BioRad, USA). Plasma hormone levels were evaluated by flow fluorimetry (Bio-PlexProteinAssaySystem, Bio-Rad, USA) using commercial test systems (Bio-PlexProHumanDiabetes 10-Plex Assay, Bio-Rad, USA). Statistical analysis and graphs were obtained at R Statistical Software. RESULTS: A violation of postprandial production of GLP-1 and ghrelin after a test breakfast in obese patients with type 2 diabetes was found. A postprandial increase in C-peptide levels of 3.25[1.83;4.16] ng/ml and insulin 3048 [1978;4972] ng/ml in carriers of the CC genotype compared with carriers of the CA genotype in the group of patients with obesity with type 2 diabetes type In carriers of the CA genotype, there was a decrease in the C-peptide level of 2.21 [1.8;2.49] ng/ml and insulin 1462 [1146; 2304] ng/ml with a constant concentration of GLP-1. The postprandial level of ghrelin in carriers of the CA genotype of the Leu260Phe polymorphism increased to 118[96.1;157] ng/ml compared to carriers of the AA 98 genotype [86; 109] ng/ml. CONCLUSION: The presence of the CC genotype of the Leu260Phe polymorphism of the GLP-1 receptor gene is associated with an increase in postprandial plasma levels of C-peptide and insulin in obese patients with type 2 diabetes, and the CA genotype with a decrease in these indicators and an increase in ghrelin content.

The role of Leu260Phe polymorphism of the receptor gene to GLP-1 incretin in the pathogenesis of diabetes type 2 diabetes with obesity

BACKGROUND: Glucagon-like peptide-1 (GLP-1) stimulates the proliferation of -cells, enhances their resistance to apoptosis and increases glucose-dependent insulin secretion.
 AIMS: Study of the relationship of Leu260Phe polymorphism (rs1042044) of the GLP-1R gene with postprandial hormone production (C-peptide, insulin, ghrelin, GLP-1) in obese patients with type 2 diabetes.
 MATERIALS AND METHODS: A total of 174 patients, 82 patients with obesity with type 2 diabetes (BMI=40.414.3 kg/m2)and 92 conditionally healthy donors (BMI=22.62.7 kg/m2) were studied. The material for the study was venous blood taken on an empty stomach and 60 minutes after the test breakfast. Genotyping was performed by PCR using the sets for determining polymorphism (rs1042044) of the GLP-1R gene (Sintol) and the amplificator (CFX96 BioRad, USA). Plasma hormone levels were evaluated by flow fluorimetry (Bio-PlexProteinAssaySystem, Bio-Rad, USA) using commercial test systems (Bio-PlexProHumanDiabetes 10-Plex Assay, Bio-Rad, USA). Statistical analysis and graphs were obtained at R Statistical Software.
 RESULTS: A violation of postprandial production of GLP-1 and ghrelin after a test breakfast in obese patients with type 2 diabetes was found. A postprandial increase in C-peptide levels of 3.25[1.83;4.16] ng/ml and insulin 3048 [1978;4972] ng/ml in carriers of the CC genotype compared with carriers of the CA genotype in the group of patients with obesity with type 2 diabetes type In carriers of the CA genotype, there was a decrease in the C-peptide level of 2.21 [1.8;2.49] ng/ml and insulin 1462 [1146; 2304] ng/ml with a constant concentration of GLP-1. The postprandial level of ghrelin in carriers of the CA genotype of the Leu260Phe polymorphism increased to 118[96.1;157] ng/ml compared to carriers of the AA 98 genotype [86; 109] ng/ml.
 CONCLUSION: The presence of the CC genotype of the Leu260Phe polymorphism of the GLP-1 receptor gene is associated with an increase in postprandial plasma levels of C-peptide and insulin in obese patients with type 2 diabetes, and the CA genotype with a decrease in these indicators and an increase in ghrelin content.

Effects of Undaria pinnatifida (Wakame) on Postprandial Glycemia and Insulin Levels in Humans: a Randomized Crossover Trial.

Postprandial hyperglycemia is a known risk factor for the development of several health disorders, including type 2 diabetes, obesity and cardiovascular disease. This study aimed to investigate the acute effect of Undaria pinnatifida (Wakame), a discriminative constituent of the Japanese diet, on postprandial blood glucose and insulin levels. The study was conducted using a crossover method among 26 subjects. Blood was sampled for glucose and insulin measurements at 0, 30, 60, 90 and 120min after a subject consumed either 200g of rice or 200g rice with 4g of dried wakame. Blood glucose and insulin levels were significantly lower at 30min after consuming rice with wakame than after consuming rice alone. Moreover, the incremental areas under the curves for glucose and insulin were lower when wakame was included. Wakame intake can improve postprandial glucose homeostasis. Wakame intake may offer a simple behavioural strategy that can reduce glycemic excursions in prediabetes. This study was registered with the UMIN Clinical Trial Registry (UMIN000031050).

Impact of energy turnover on the regulation of glucose homeostasis in healthy subjects

ObjectiveSedentary lifestyle increases the risk of type 2 diabetes. The aim of this study was to investigate the impact of different levels of energy turnover (ET; low, medium, and high level of physical activity and the corresponding energy intake) on glucose metabolism at zero energy balance, caloric restriction, and overfeeding.MethodsSixteen healthy individuals (13 men, 3 women, 25.1 ± 3.9 years, BMI 24.0 ± 3.2 kg/m2) participated in a randomized crossover intervention under metabolic ward conditions. Subjects passed 3 × 3 intervention days. Three levels of physical activity (PAL: low 1.3, medium 1.6, and high 1.8 achieved by walking at 4 km/h for 0, 3 × 55, or 3 × 110 min) were compared under three levels of energy balance (zero energy balance (EB): 100% of energy requirement (Ereq); caloric restriction (CR): 75% Ereq, and overfeeding (OF): 125% Ereq). Continuous interstitial glucose monitoring, C-peptide excretion, and HOMA–IR, as well as postprandial glucose and insulin were measured.ResultsDaylong glycemia and insulin secretion did not increase with higher ET at all conditions of energy balance (EB, CR, and OF), despite a correspondingly higher CHO intake (Δ low vs. high ET: +86 to 135 g of CHO/d). At CR, daylong glycemia (p = 0.02) and insulin secretion (p = 0.04) were even reduced with high compared with low ET. HOMA–IR was impaired with OF and improved with CR, whereas ET had no effect on fasting insulin sensitivity. A higher ET led to lower postprandial glucose and insulin levels under conditions of CR and OF.ConclusionLow-intensity physical activity can significantly improve postprandial glycemic response of healthy individuals, independent of energy balance.

Evaluation of high nutrient diets and additional dextrose on reproductive performance and litter performance of heat-stressed lactating sows.

This study investigated the litter performance of lactating sows fed nutrient-dense diets with or without dextrose at farrowing to weaning, during the summer with an average room temperature of 28.4°C. A total of 60 (13 first parity, 13 second parity, 19 third parity, and 15 forth parity) cross-bred sows were assigned to three treatments. The three treatments were: standard diet (ST), high nutrient diet (HN; ST+3% higher energy and 18.0% protein), and high nutrient diet plus dextrose (HND; 3% higher energy, 18.0% protein, and 5% dextrose). BW loss was reduced in the HND sows compared with the ST sows during lactation. The HN and HND sows had a higher piglet and litter weight at weaning. Also, the HND sows had the highest post-prandial insulin levels at weaning and the shortest weaning-to-service interval (WSI). Serum LH was higher in the HND sows than the ST sows. The milk fat level was higher in the HND sows compared with the ST sows, but similar to the HN sows. In conclusion, these results suggest that it is possible to increase the blood insulin response by supplementing dextrose to a high nutrient diet, thus, improving WSI interval and litter growth during heat stress.

Effect of acute bitter melon intake on postprandial glucose and insulin in sedentary, abdominally obese persons

Background: Lifestyle modifications have been considered to be the primary prevention strategies for diabetes. However, there is a lack of evidence guiding the use of functional food sthat potentially possess anti-hyperglycemic effects. The objective of this study was to investigate the acute effect of bitter melon intake on postprandial glucose and insulin levels in sedentary, abdominally obese persons.Methods: In this study, 16 sedentary, abdominally obese participants were randomly assigned to receive either 100 ml of bitter melon juice or placebo juice 30 minutes prior to an oral glucose tolerance test. Plasma glucose and serum insulin were measured every 30 minutes during the 2-hour postprandial period. Two-way repeated measure ANOVA was used to test the effects of bitter melon on postprandial glucose and insulin levels after adjustment for covariates.Results: The 2-h postprandial glucose was significantly lower in bitter melon group as compared with control group (99.5 ± 22.3 vs 133.9 ± 36.9 mg/dL, P=0.04), resulting in an absolute glucose reduction of 34.4 mg/dL (95% confidence interval, 1.7 to 67.1 mg/dL) and a relative glucose reduction of 26%. There was a fairly significant reduction in 2-h postprandial glucose incremental area under the curve (iAUC) (52.9 ± 29.5 vs 94.7 ± 47.3 mg/dL·h, P=0.052), resulting in a relative glucose reduction of 44%.Conclusion: Our acute study demonstrated that the single-dose intake of bitter melon juice decreased postprandial glucose levels among sedentary, abdominally obese persons. Bitter melon juice appears to be a promising functional food to manage hyperglycemia for people who are at elevated risk of developing diabetes.Key Words: Functional Food; Momordica Charantia; Hyperglycemia; Sedentary; Obese

Differential effects of a 40-hour fast and bile acid supplementation on human GLP-1 and FGF19 responses.

Bile acids, glucagon-like peptide-1 (GLP-1), and fibroblast growth factor 19 (FGF19) play an important role in postprandial metabolism. In this study, we investigated the postprandial bile acid response in plasma and its relation to insulin, GLP-1, and FGF19. First, we investigated the postprandial response to 40-h fast. Then we administered glycine-conjugated deoxycholic acid (gDCA) with the meal. We performed two separate observational randomized crossover studies on healthy, lean men. In experiment 1: we tested 4-h mixed meal after an overnight fast and a 40-h fast. In experiment 2, we tested a 4-h mixed meal test with and without gDCA supplementation. Both studies measured postprandial glucose, insulin, bile acids, GLP-1, and FGF19. In experiment 1, 40 h of fasting induced insulin resistance and increased postprandial GLP-1 and FGF19 concentrations. After an overnight fast, we observed strong correlations between postprandial insulin and gDCA levels at specific time points. In experiment 2, administration of gDCA increased GLP-1 levels and lowered late postprandial glucose without effect on FGF19. Energy expenditure was not affected by gDCA administration. Unexpectedly, 40 h of fasting increased both GLP-1 and FGF19, where the former appeared bile acid independent and the latter bile acid dependent. Second, a single dose of gDCA increased postprandial GLP-1. Therefore, our data add complexity to the physiological regulation of the enterokines GLP-1 and FGF19 by bile acids.